To further examine the "estrogenicity" of chlorinated hydrocarbons, the effect of these compounds on the activity of uterine ornithine decarboxylase (OD) was determined. The administration of chlorinated hydrocarbons to female rats markedly elevated uterine OD but not liver OD, demonstrating organ specificity. The order of decreasing potency in causing OD elevation was: o,p'DDT greater than o,p'DDD greater than p,p'DDD; a similar order of uterotropic potency of these compounds was previously shown. The increase in uterine OD by o,p'DDT was inhibited by co-administration of inhibitors of protein synthesis suggesting that o,p'DDT caused a de novo enzyme formation. A direct attempt to demonstrate that o,p'DDT binds to the S8 uterine estrogen receptor failed, presumably the specific activity of the radiolabeled o,p'DDT was not sufficiently high for detection. However, evidence which suggests such binding was indirectly obtained. o,p'DDT was found to inhibit markedly the binding of radiolabeled estradiol to the S8 uterine receptor from mice and rats. This suggests that chlorinated hydrocarbons act similarly to steroidal estrogens. Obviously, the possibility that o.p'DDT merely inactivates the receptor has not been ruled out.